Comparison of surgical outcomes of sleep surgeries preoperatively evaluated with drug-induced sleep endoscopy and Müller's maneuver.

Objective The purpose of this study was to compare surgical outcomes for obstructive sleep apnea (OSA) when the procedure was based on the results of drug-induced sleep endoscopy (DISE) vs. the awake Müller's maneuver (MM). Methods Forty-seven patients with OSA who underwent sleep surgery were included. Patients were divided into 2 groups according to their preoperative upper airway evaluation method. Twenty-five patients received only MM for surgical decision making (MM group), and 22 patients received both MM and DISE (DISE group) for surgical decision making. Results The surgical success rate of the DISE group was higher than that of the MM group (59% vs. 36%), but the difference was not significant (p = 0.118). The differences between pre- and postoperative apnea-hypopnea index (AHI) values in both the MM and DISE group were highly significantly different (p < 0.001). Fifteen patients in the DISE group (68.2%) received multi-level surgery, while in the MM group only 7 patients (28%) received multi-level surgery. Patients with more severe OSA (AHI > 22 or lowest O2 saturation < 81%) had better surgical outcomes when their surgical procedures were based on the findings of DISE, rather than those of MM. Conclusion The results indicate that DISE provides no benefits with respect to surgical outcomes for patients with mild to moderate OSA; however, for patients with more severe OSA surgical procedures based on DISE result in better outcomes.

MicroRNA-145-5p modulates Krüppel-like factor 5 and inhibits cell proliferation, migration, and invasion in nasopharyngeal carcinoma.

BACKGROUND: In several human cancers, Krüppel-like factor 5 (KLF5), a zinc finger transcription factor, can contribute to both tumor progression or suppression; however, the precise role of KLF5 in nasopharyngeal carcinoma (NPC) remains poorly understood. In this study, the association between KLF5 and microRNA-145-5p (miR-145-5p) in NPC cells was elucidated. RESULTS: Our results showed that KLF5 expression was up-regulated in NPC group compared to normal group. We found that KLF5 exhibited an oncogenic role in NPC cells. The upregulation of miR-145-5p inhibited the proliferation, migration, and invasion of NPC cells. It was observed that miR-145-5p could down-regulate the mRNA and protein expression of KLF5 in NPC cell lines. Additionally, the activity of focal adhesion kinase (FAK), a migration marker, was regulated by miR-145-5p and KLF5 in NPC cells. CONCLUSIONS: The results of this study indicated that miR-145-5p could repress the proliferation, migration, and invasion of NPC cells via KLF5/FAK regulation, and could be a potential therapeutic target for patients with NPC.

The antimicrobial peptide tilapia piscidin 3 induces mitochondria-modulated intrinsic apoptosis of osteosarcoma cells.

Osteosarcoma (OS) is the most common solid tumor of the bone that most often affects adolescents. The introduction of chemotherapy for the treatment of OS has largely improved the survival rates of patients with localized tumors. However, the 5-year survival rate of OS patients with relapsed or metastatic disease is only 10 to 20%. In this study, the antimicrobial peptide tilapia piscidin 3 (TP3), isolated from Nile tilapia (Oreochromis niloticus), was treated to OS MG63 cells. Our findings showed that TP3 concentration as low as 1 µM induced significant inhibition of cell viability and increased DNA fragmentation, as determined by the MTT and TUNEL assays, respectively. The protein expression levels of cleaved caspases 3/9 were increased. An in situ live-cell time-lapse video and cell tomographic microscopy images showed cellular blebbing, shrinkage, nuclear fragmentation, and chromatin condensation, with the formation of beaded apoptopodia. Moreover, there were significant increase in the production of TP3-induced mitochondrial and cellular reactive oxygen species (ROS), as well as down-regulated mitochondrial oxygen consumption and extracellular acidification rates. Additionally, TP3 enhanced mitochondrial fission, whereas fusion was attenuated. Furthermore, after administration of the mitochondria targeted antioxidant mitoTempo, TP3-induced ROS oxidant levels and alterations in cleaved caspases 3/9 expression were rescued. TP3 promoted mitochondria-modulated intrinsic apoptosis through the induction of ROS production, activation of caspases 3/9, and the down-regulation of mitochondrial oxygen consumption and extracellular acidification rates, suggesting that TP3 has potential as an innovative alternative for OS treatment.